OASL1 Traps Viral RNAs in Stress Granules to Promote Antiviral Responses

  • Kang, Ji-Seon (Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University) ;
  • Hwang, Yune-Sahng (Department for Integrated OMICs for Biomedical Science, Yonsei University) ;
  • Kim, Lark Kyun (Severance Biomedical Science Institute and BK21 PLUS project to Medical Sciences, Gangnam Severance Hospital, Yonsei University College of Medicine) ;
  • Lee, Sujung (Department of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University) ;
  • Lee, Wook-Bin (Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University) ;
  • Kim-Ha, Jeongsil (Department of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University) ;
  • Kim, Young-Joon (Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University)
  • Received : 2017.11.08
  • Accepted : 2017.12.17
  • Published : 2018.03.31


Oligoadenylate synthetase (OAS) protein family is the major interferon (IFN)-stimulated genes responsible for the activation of RNase L pathway upon viral infection. OAS-like (OASL) is also required for inhibition of viral growth in human cells, but the loss of one of its mouse homolog, OASL1, causes a severe defect in termination of type I interferon production. To further investigate the antiviral activity of OASL1, we examined its subcellular localization and regulatory roles in IFN production in the early and late stages of viral infection. We found OASL1, but not OASL2, formed stress granules trapping viral RNAs and promoted efficient RLR signaling in early stages of infection. Stress granule formation was dependent on RNA binding activity of OASL1. But in the late stages of infection, OASL1 interacted with IRF7 transcripts to inhibit translation resulting in down regulation of IFN production. These results implicate that OASL1 plays context dependent functions in the antiviral response for the clearance and resolution of viral infections.


Supported by : NRF


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